Chronic renal failure is the primary cause of secondary hyperparathyroidism (SHPT). Patients with mineral metabolism disorders commonly present with low serum calcium levels, hyperphosphatemia, and calcitriol deficiency. In normal renal function subjects, parathyroid cells have a low turnover and rarely undergo mitoses. In uremic conditions, however, parathyroid glands become hyperplasic and leave quiescence. During the last ten years, new molecular mechanisms have been investigated to better understand the pathogenesis of SHPT: the emerging role of the Calcium Sensing Receptor (CaSR); the importance of the parathyroid expression of the Vitamin D receptor (VDR); the growing evidence on the central role of the Fibroblast Growth Factor 23 (FGF-23). In contrast, the discovery of a parathyroid phosphate sensor or receptor has yet to be made.

Pathogenesis of secondary hyperparathyroidism / M.G. Cozzolino, S. Pasho, G. Fallabrino, L. Olivi, M.A. Gallieni, D. Brancaccio. - In: INTERNATIONAL JOURNAL OF ARTIFICIAL ORGANS. - ISSN 0391-3988. - 32:2(2009 Feb), pp. 75-80.

Pathogenesis of secondary hyperparathyroidism

M.G. Cozzolino
Primo
;
M.A. Gallieni
Penultimo
;
D. Brancaccio
Ultimo
2009

Abstract

Chronic renal failure is the primary cause of secondary hyperparathyroidism (SHPT). Patients with mineral metabolism disorders commonly present with low serum calcium levels, hyperphosphatemia, and calcitriol deficiency. In normal renal function subjects, parathyroid cells have a low turnover and rarely undergo mitoses. In uremic conditions, however, parathyroid glands become hyperplasic and leave quiescence. During the last ten years, new molecular mechanisms have been investigated to better understand the pathogenesis of SHPT: the emerging role of the Calcium Sensing Receptor (CaSR); the importance of the parathyroid expression of the Vitamin D receptor (VDR); the growing evidence on the central role of the Fibroblast Growth Factor 23 (FGF-23). In contrast, the discovery of a parathyroid phosphate sensor or receptor has yet to be made.
Calcium; Phosphate; PTH; Renal failure; Vitamin D
Settore MED/14 - Nefrologia
feb-2009
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/69243
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